Fibroblast Growth Factor-23: A Novel Biomarker for Cardiovascular Disease in Chronic Kidney Disease Patients
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Updated: Feb 21, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Insights
Elevated Fibroblast Growth Factor (FGF)-23 is an early sign in chronic kidney disease-mineral bone disorder (CKD-MBD). This FGF-23 increase is linked to higher cardiovascular risks in CKD patients, prompting research into its mechanisms and therapeutic potential.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Fibroblast Growth Factor (FGF)-23 elevation is an early biomarker in chronic kidney disease-mineral bone disorder (CKD-MBD).
- Growing evidence links increased FGF-23 to cardiovascular morbidity and mortality in CKD and other populations.
- The precise cardiovascular effects of FGF-23 are under intense investigation.
Purpose of the Study:
- To explore the cellular and molecular mechanisms of FGF-23's detrimental cardiovascular effects.
- To investigate the interactions between FGF-23 and known cardiovascular risk factors.
- To determine if FGF-23 is a modifiable risk factor and a potential therapeutic target in CKD.
Main Methods:
- Review of animal and human studies on FGF-23 actions in the heart and vasculature.
- Analysis of reported interactions between FGF-23, renin-angiotensin system, and inflammation.
- Examination of clinical data associating FGF-23 with adverse outcomes.
Main Results:
- FGF-23 exerts significant actions on the heart and blood vessels, potentially contributing to cardiovascular complications in uremia.
- Interactions with the renin-angiotensin system and inflammation may partially explain FGF-23's association with poor clinical outcomes.
- Studies demonstrate a link between elevated FGF-23 and increased cardiovascular risk.
Conclusions:
- Further research is required to elucidate the pleiotropic actions of FGF-23.
- Identifying FGF-23 as a modifiable risk factor could lead to new therapeutic strategies.
- Targeting FGF-23 may help reduce the high cardiovascular burden in CKD patients.
Abstract:
Fibroblast Growth Factor (FGF)-23 increase is considered one of the earliest biochemical abnormalities in chronic kidney disease-mineral bone disorder (CKD-MBD). Furthermore, accumulating data have provided evidence of a link between increased FGF-23 levels and cardiovascular morbidity and mortality in CKD patients as well as in several other populations including cardiology patients and general population. The cellular and molecular mechanisms underlying the deleterious effect of FGF-23 on the cardiovascular system are not yet completely defined and are the focus of intense research. However, animal and human studies have demonstrated important actions of FGF-23 in the heart and vessels through which could promote the development of cardiovascular complications in uremia. Moreover, significant interactions have been reported between FGF-23 and other well recognized cardiovascular risk factors such as renin-angiotensin system and inflammation which could account, at least in part, for the observed associations between FGF-23 and adverse clinical outcomes. Further studies are needed to clarify the mechanisms responsible for the pleiotropic actions of FGF-23 and moreover to identify whether it is a modifiable risk factor and a potential target of therapeutic interventions which could probably help to reduce the unacceptably high cardiovascular morbidity and mortality of CKD patients.
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